Molecular and Cellular Mechanisms Underlying Neurodegenerative Disorders

Submission Deadline: 31 August 2026 View: 55 Submit to Special Issue

Guest Editors

Dr. Luciano Porto Kagami

Email: lucianopkagami@outlook.com

Affiliation: Laboratório de Síntese Orgânica Medicinal - LaSOM®, Programa de Pós-Graduação em Ciências Farmacêuticas, Faculdade de Farmácia, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil

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Research Interests: cell biology, molecular biology, stem cells, cancer biology, immunology, genomics, biotechnology

Dr. Aamir Saeed Malik

Email: malik@fit.vutbr.cz 

Affiliation: Faculty of Information Technology, Brno University of Technology, Brno, 61200, Czech Republic

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Research Interests: EEG, Machine Learning, Brain–Computer Interface, Mental Health Detection, Cognitive Neuroscience, Biomedical Signal Processing, Image Processing

Dr. Francisco Javier Ramírez-Arias

Email: francisco.javier.ramirez.arias@uabc.edu.mx 

Affiliation: Facultad de Ingeniería, Arquitectura y Diseño, Universidad Autónoma de Baja California, Carretera Transpeninsular Ensenada-Tijuana No. 3917, Ensenada 22860, Mexico

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Research Interests:  EEG, brain-computer interface, motor imagery, biomedical signal processing, machine learning, neurorehabilitation

Summary

Molecular and cellular mechanisms into neurodegeneration have become central to understanding how disruptions in protein homeostasis, intracellular signalling, membrane dynamics, synaptic integrity and neuron-glia interactions collectively drive in the gradual loss of neural function. The basic cell biology findings in neurochemistry and molecular genetics have shown that abnormal protein folding, inefficient clearance pathways, excitotoxicity, mitochondrial failure, oxidative stress and chronic neuroinflammation are interconnected processes that destabilize neuronal survival and plasticity. These mechanisms act at the macromolecular organization level, influencing cytoskeletal structure, vesicular transport, membrane composition and gene regulatory networks which ensure cellular identity and functionality. In this framework, molecular profiling, proteomic and transcriptomic mapping, single-cell analysis, live-cell imaging of regulatory events and functional assays of glial activation are some of the applications that have been used to identify cell-specific vulnerabilities and disease-driving biochemical transitions. These methods have significant benefits of recording early molecular disturbances, clarifying crosstalk in neurons, microglia and astrocytes enabling the dissection of pathways that regulate survival signalling, synaptic maintenance and innate immune responses.

 
Regardless of these strengths, challenges persist, such as the complexity of overlapping degenerative cascades, inability to isolate cell-type-specific contributions in heterogeneous tissues, limited in vitro models that recapitulate human neural microenvironments and the incomplete knowledge of how metabolic stress, genetic variation and epigenetic regulation interact to define disease susceptibility. Future perspectives highlight the combination of multi-omics data, high-resolution cellular models, advanced molecular perturbation tools and computational systems biology to build mechanistic maps linking molecular dysregulation to cell-level phenotypes. The further understanding of how non-coding RNAs, chromatin structure, lipid signalling, ion channel dynamics and intracellular trafficking affect degenerative progression will help to improve the knowledge of regulatory networks that support neurobiology. Ultimately, emphasis on core cellular and molecular processes will offer a basis on which to define early pathological signatures, therapeutic targets and enhance conceptual models of neural dysfunction and all of which is consistent with the focus on the biochemical and structural basis of cell behavior in neurodegenerative conditions.

The aim of this collection is to submit contributions that strengthen the understanding of how molecular pathways, regulatory networks and cell-level dynamics establish and develop neurodegenerative conditions. We invite submissions emphasizing innovative insights into neuronal-glial interactions, protein homeostasis, intracellular signalling disturbances and biochemical processes driving cellular dysfunction. The collection encourages research integrating molecular biology, neurochemistry, cell dynamics and mechanistic modeling including theoretical work that can help refine current concepts of neural degeneration. Submissions that advance knowledge of core cellular mechanisms and expand the biological basis of neurodegenerative pathology are particularly appreciated.

We welcome articles exploring topics including, but not limited to:
• Single-Cell Multi-Omics Mapping of Cellular Pathways Driving Neurodegenerative Progression
• Proteomic Signatures of Synaptic Breakdown and Neuron-Glia Dysregulation in Neurodegeneration
• Epigenetic Control of Neuronal Vulnerability Through Chromatin and Transcriptional Rewiring
• Machine-Learning Integration of Molecular Markers Predicting Early Degenerative Phenotypes
• Computational Network Modeling of Cellular Pathways Regulating Neurodegenerative Cascades
• Advanced Fluorescence Microscopy of Intracellular Trafficking Disruptions in Neural Cells
• Non-Coding RNA Regulation of Neuronal Plasticity and Degeneration-Associated Signalling
• Phosphoproteomic Analysis of Dysregulated Cell Signalling in Neurodegenerative Disorders
• Organoid Models Revealing Cellular Dynamics of Human Neurodegenerative Pathophysiology
• Cytoskeletal Remodelling Mechanisms Affecting Axonal Stability During Degenerative Processes
• Bioinformatic Reconstruction of Pathway Interactions Underlying Progressive Neural Damage
• Membrane Receptor Dysregulation and Synaptic Signalling Failure in Degenerative Diseases

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